PD-L1 is induced in hepatocytes by viral infection and by interferon-α and -γ and mediates T cell apoptosis

Mühlbauer, Marcus; Fleck, Martin; Schütz, Christian; Weiss, Thomas; Froh, Matthias; Blank, Christian; Schölmerich, Jürgen; Hellerbrand, Claus

doi:10.1016/j.jhep.2006.05.007

Cited by 378Cancer Immunotherapy and BiomarkersLiver Diseases and ImmunityT-cell and B-cell Immunology

PD-L1 is induced in hepatocytes by viral infection and by interferon-α and -γ and mediates T cell apoptosis

Mühlbauer, Marcus, Fleck, Martin, Schütz, Christian, Weiss, Thomas, Froh, Matthias, Blank, Christian, Schölmerich, Jürgen, Hellerbrand, Claus·2006·Journal of Hepatology

DOI 10.1016/j.jhep.2006.05.007

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Abstract

Background/aims B7-H1 (PD-L1) is a B7-family member that binds to programmed death-1 (PD-1). Recently, deficiency of PD-L1 has been demonstrated to result in accelerated hepatocyte damage in experimental autoimmune hepatitis, and PD-L1 was suggested to play a critical role in regulating T cell homeostasis. Absence of PD-1 enhanced proliferation of T cells in adenovirus-infected livers and resulted in a rapid clearance of the virus. Here, we aimed to get more insight into hepatic PD-L1 expression, regulation and function. Methods PD-L1 expression was analyzed by quantitative PCR and FACS-analysis in primary human liver cells and hepatoma cells. Furthermore, coculture experiments with primary human T cells or Jurkat T cells were established. Results In addition to nonparenchymal liver cells, also hepatocytes constitutively expressed low levels of PD-L1. PD-L1 expression in hepatocytes was strongly enhanced by activated T cells and viral infection, and markedly augmented by further stimulation with type I or type II interferons. Moreover, PD-L1 expression on hepatocytes induced apoptosis in T cells. Conclusions Our results suggest a novel bidirectional interaction between hepatocytes and lymphocytes modulated by PD-L1 expression in hepatocytes, which may contribute to the unique immunological properties of the liver.

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MHC class II antigen presentation by hepatocytes cannot trigger effective activation of T cells, and in turn might favour a chronic viral infection over viral clearance.
“This evidence suggests that the fate of MHC class II antigen presentation by the hepatocyte cannot trigger an effective activation of the T cells, and in turn it might favour a chronic viral infection over viral clearance(31, 39-41).”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [39]
Constitutive expression of MHC class II on hepatocytes in murine models of choriomeningitis virus infection increases the duration of the infection and reduces production of pro-inflammatory cytokines (IFN-γ) by virus-specific CD4+ and CD8+ T cells.
“Constitutive expression of MHC class II on hepatocytes in murine models of choriomeningitis virus infection has shown to increase the duration of the infection, reducing the production of pro-inflammatory cytokines (i.e. IFN-γ) by virus-specific CD4 + T and CD8 + T cells.”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [39]
A sizeable proportion, between 23% and 48%, of patients with MASLD and/or MASH were found to exhibit signs of AIH and/or PBC, including interface hepatitis and generation of anti-nuclear or anti-mitochondrial antibodies.
“In the small number of investigations performed, a sizeable proportion (between 23% and 48%) of patients with MASLD and/or MASH were found to exhibit signs of AIH and/or PBC, including interface hepatitis and generation of anti-nuclear (ANA) or anti-mitochondrial (AMA) antibodies (38-40).”
From The liver as a central "hub" of the immune system: pathophysiological implications (2025) · cites this paper as [39]

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Authors: Mühlbauer, M., Fleck, M., Schütz, C., Weiss, T., Froh, M., Blank, C., Schölmerich, J., & Hellerbrand, C.
Affiliations: University of Regensburg (DE)
ORCID: Mühlbauer, Marcus
Fleck, Martin
Schütz, Christian
Weiss, Thomas
Blank, Christian
Hellerbrand, Claus
Venue: Journal of Hepatology
Publisher: Elsevier BV
Published: 2006-10
Volume: 45
Issue: 4
Pages: 520-528
ISSN: 0168-8278 (ISSN-L)
DOI: 10.1016/j.jhep.2006.05.007
OpenAlex: W2070715664
Cited by: 378
References: 47
Citations by year: 2026: 7 · 2025: 14 · 2024: 13 · 2023: 21 · 2022: 12 · 2021: 24 · 2020: 30 · 2019: 19 · 2018: 21 · 2017: 26 · 2016: 20 · 2015: 27 · 2014: 12 · 2013: 13 · 2012: 17
FWCI: 11.62
Type: journal article
Language: en
Open access: closed
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Journal of Hepatology (publishedVersion)
PubMed (publishedVersion)
University of Regensburg Publication Server (University of Regensburg) (submittedVersion)
Funders: Wilhelm Sander-Stiftung
Universität Regensburg
Topics: Health Sciences › Medicine › Oncology › Cancer Immunotherapy and Biomarkers
Health Sciences › Medicine › Hepatology › Liver Diseases and Immunity
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: PD-L1, hepatocytes, viral infection, interferon-alpha, interferon-gamma, T cell apoptosis, PD-1, liver immunology, adenovirus infection, hepatocyte injury
MeSH terms: Adenovirus Infections, Human, Cell Communication, Humans, Interferon-gamma, Liver, Lymphocyte Activation, RNA, Messenger, T-Lymphocytes, Tumor Cells, Cultured, Antigens, CD, Gene Expression, Interferon-alpha, Apoptosis, Coculture Techniques, Jurkat Cells, Hepatocytes, B7-H1 Antigen

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PD-L1 is induced in hepatocytes by viral infection and by interferon-α and -γ and mediates T cell apoptosis

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